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Mithramycin A Inhibits Colorectal Cancer Growth by Targeting Cancer Stem Cells

Waise Quarni1,2, Rinku Dutta1,2, Ryan Green1,2

  • 1Department of Molecular Medicine, Morsani College of Medicine, University of South Florida, Tampa, FL, 33612, USA.

Scientific Reports
|October 25, 2019
PubMed

Insights

Mithramycin A (Mit-A) shows promise as a total cancer therapy drug by inhibiting both cancer stem cells (CSCs) and bulk cancer cells in colorectal cancer models. This study identifies Mit-A as a potential treatment targeting CSCs and bulk tumor cells for improved CRC therapy.

Area of Science:

  • Oncology
  • Cancer Stem Cell Biology
  • Drug Discovery

Background:

  • Cancer initiating stem cells (CSCs) drive tumor growth, metastasis, and drug resistance, necessitating therapies targeting both CSCs and bulk cancer cells.
  • Current therapeutic strategies often fail to eradicate CSCs, leading to relapse and treatment failure in colorectal cancer (CRC).
  • Developing effective 'total cancer therapy' requires identifying novel agents that can simultaneously target diverse cancer cell populations.

Purpose of the Study:

  • To identify novel FDA-approved drugs capable of inhibiting both cancer cells and CSCs in colorectal cancer.
  • To evaluate the efficacy of mithramycin A (Mit-A) as a potential 'total cancer therapy' agent against CRC.
  • To investigate the mechanisms by which Mit-A exerts its anti-cancer effects in CRC models.

Main Methods:

  • Established 3D tumor organoid (tumoroid) models from CRC cell lines and ex vivo mouse tumors using a polymeric nanofiber scaffold.
  • Screened the NCI library of FDA-approved drugs to identify potential therapeutic candidates.
  • Assessed the effects of Mit-A on CSC markers, proliferation, SP1 expression, tumoroid growth, and in vivo tumor growth in CRC models.
  • Evaluated Mit-A's impact on cell death and PARP-cleavage in both CSC and non-CSC populations.

Main Results:

  • Mit-A demonstrated significant inhibition of CSC proliferation and bulk cancer cell growth in CRC models.
  • Mit-A reduced the expression of cancer stemness markers and SP1 in CRC tumoroids and cells.
  • In vivo studies showed that Mit-A significantly reduced CRC tumor growth and induced cell death in both CSC and non-CSC populations.

Conclusions:

  • Mithramycin A is identified as a promising drug candidate for total cancer therapy in colorectal cancer.
  • Mit-A effectively targets both cancer stem cells and bulk cancer cells, addressing a critical need in CRC treatment.
  • The findings support further investigation of Mit-A as a therapeutic agent for improving outcomes in colorectal cancer patients.

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